The supernatant of cervical carcinoma cells lines induces a decrease in phosphorylation of STAT

Macrophages are presents in the tumor microenvironment and acquire different phenotypic and functional characteristics in response to microenvironmental signals. Macrophages can be differentiated into two phenotypes: M1 or pro-inflammatory (classically activated), and M2 or anti-inflammatory macrophage (alternatively activated). In response to the microenvironment, macrophages activate transcription factors as STAT1 and NF-κB-p65 for M1 macrophages or STAT3 and STAT6 for M2 macrophages; activation impacts on the profile of cytokine, chemokines and growth factors secreted by macrophages. We evaluated the effect of the supernatant of cervical-derived carcinoma cell lines HeLa, SiHa, and C-33A on the phosphorylation of transcriptional factors STAT1, NF-κB-p65, and STAT6, and their impact in the profile of secretion of cytokines and growth factors by macrophages derived from the U937 cell line. The results show that in macrophages, these supernatants induce a decrease in the phosphorylation of NF-κB-p65 and STAT1 in U937-macrophages accompanied by an increase in the secretion of IL-10, IL-6, MCP-1, and IL-8, as well as GM-CSF, G-CSF, PDGF-AA, PDGF-BB, and VEGF. Our results suggest that HeLa, SiHa, and C-33A cell lines down-regulate the activation of transcription factors characteristic of M1 macrophages (STAT1, NF-κB-p65) and induce the secretion of factors that favor tumor growth